1. Field of the Invention
The present invention relates generally to ventilators for supporting ventilation in air breathing animals. More particularly, the present invention relates to high frequency ventilators which operate by oscillating respiratory air supplied to a patient at a frequency above the normal breathing frequency of the patient.
2. Discussion of Related Art
The use of a medical apparatus to facilitate breathing in mammals is well known in the art. The apparatus may take the form of a simple oxygen mask or tent which supplies oxygen at slightly above atmospheric pressure. Such devices merely assist a person to breathe.
Ventilators which operate at a high frequency have been suggested in the past. There are three types of high frequency ventilators known in the art, the flow interrupter, the jet ventilator and the high frequency oscillating ventilator. The latter, as exemplified by U.S. Pat. No. 2,918,917 to Emerson, employs a reciprocating diaphragm to vibrate a column of gas supplied to a patient. The vibration is in addition to the subject's respiration, natural or artificial, and at a much more rapid rate, for example, from 100 to more than 1500 vibrations per minute. The Emerson apparatus is primarily designed to vibrate the patient's airway and organs associated therewith, although Emerson also recognized that high frequency vibration causes the gas to diffuse more rapidly within the airway and therefore aids the breathing function. However, the Emerson apparatus is incapable of supporting full ventilation of the patient and must be used in conjunction with the patient's spontaneous breathing or with another apparatus which produces artificially induced inhalation and exhalation.
The second type of high frequency ventilator, the flow interrupter, uses a valve to switch a high pressure source of gas on and off. There are three disadvantages to such a device. First, there is the hazard of having the valve stick in the open position, thereby exposing the patient to very high pressure. The other problems relate to the fact that the respiratory gas enters the trachea at high speed. The high speed causes erosion and burning of the trachea at the point of entry. Further, all the external energy applied to the patient is toward inspiration, driving mucus and secretions down further into the lungs and relying solely on the compliance of the lungs and chest muscles for expiration. Consequently, the flow interrupter is of little value at frequencies over 3 Hz, which is the approximate limit of compliance of the lungs and chest muscles.
A third type of high frequency ventilator is the jet pulse ventilator as exemplified in U.S. Pat. No. 4,265,237 to Schwanbom et al. The Schwanbom et al. ventilator produces high frequency, high pressure pulses of air which are capable of fully ventilating a patient. According to the specification of that patient, the respiration pulse developed by that ventilator arrives at the closing valve with a pressure of 0.2 bar (209 cm H.sub.2 O) to 2.7 bar (2797.2 cm H.sub.2 O). This pressure is sufficient to expand the lungs during inspiration. Expiration is caused by the natural compliance of the lungs and chest rebound after the jet of air is stopped. Accordingly, it can be seen that the device described in the Schwanbom et al. patent must rely on the compliance of the lungs in order to ventilate the patient. If the lung compliance is low, greater pressure must be used. The device described in the Schwanbom et al. patent also supplies a source of lower pressure gas for spontaneous breathing by the patient. While such jet pulse ventilators are useful for some applications, they are not generally applicable and their use is limited to certain applications. For instance, when used to support the respiration of neonates, as, for instance, those suffering from hyaline membrane disease, the baby often suffers substantial injury to the airway due to erosion caused by the impact of the high velocity jet of gas on the airway. Further, like the flow interrupter, all the energy applied to the patient is during inspiration, causing secretions to be driven down into the lungs.
U.S. Pat. No. 4,155,356 to Venegas discloses a respiration assisting apparatus using high frequency pulses to hold a patient's airway open while the patient is breathing or being ventilated with a volume ventilator. As with the Emerson device, Venegas is not capable of fully supporting a patient and must rely either on the natural respiration cycle or on a volume type ventilator to sustain the patient.
It is believed that normal breathing functions of air breathing animals are caused by expansion of the chest cavity. The expansion puts a negative pressure on the outside of the plurality of alveolar sacs in the lungs. The innumerable alveolar sacs receive air from the tidal flow or air movements generated, replenishing the sacs with oxygen-containing gas and removing carbon dioxide-containing gas. The intake of oxygen into the body is referred to as oxygenation, and the elimination of carbon dioxide from the body is referred to as ventilation. The compliance of the alveolar sacs causes them to inflate and deflate in response to the pressure changes.
When the chest cavity expands and creates a negative pressure on the outside of the alveolar sacs, it is believed this causes the sacs to inflate and provides movement of air into the alveolar sacs due to the pressure change. In order to exhale, the pressure on the outside of the alveolar sacs is increased by relaxing the chest cavity, allowing the elastic alveolar sacs to reduce their size and allowing expiration.
As far as is known, commercially available prior art ventilators use a relatively high positive air pressure to inflate the lungs like a balloon until either a predetermined volume of air is delivered to the patient or a predetermined pressure is reached. The operation and use of conventional mechanical ventilators is summarized in Kestner, J., "The Mechanical Ventilator", in C. C. Rattenborg (Ed.), Clinical Use of Mechanical Ventilation, Year Book Medical Publishers, Inc. (1981), pp. 46-60. If too much volume or pressure is utilized, the compliance or elasticity of the alveolar sacs is reduced. Eventually, the damage will become so extensive that the sacs will no longer function to expel gas and thereby provide oxygen and carbon dioxide exchange.
When a patient is hooked up to a ventilator, blood gases are monitored to determine whether sufficient oxygenation and ventilation is occuring at the alveolar sacs. When the blood gases deteriorate, present ventilators must correct the problem by increasing the pressure of the gas flowing into the lungs, the increase in pressure affects the compliance and elasticity of the sacs even more and can eventually destroy the lungs. A person essentially becomes dependent upon the ventilator and must gradually be weaned from the ventilator.
When the patient's lungs are not diseased, a low inspiratory pressure can be used because the lungs can expand and contract on their own to provide volume exchange of gases in the alveolar sacs. When there is lung disease present, it may not be possible for the lungs to provide adequate ventilation or gas exchange in the alveolar sacs. This requires some means of facilitating the gas exchange.
The failure of ventilation in conventionally available ventilators generally begins with expiration failures. As mentioned earlier, the conventional method for increasing gas exchange when blood gases deteriorate is to increase the pressure of the gas flowing into the lungs. The lungs can sustain a slight over-pressuring for a short period of time and not incur permanent damage. However, continued over-pressuring will cause a change in the compliance of the alveolar sacs. A bleb or rupture can occur when the alveolar sac has exceeded its elastic limit. Hemorrhaging may result, which destroys the ability of the sac to effect gas exchange and may cause other complications.
During normal breathing, it is believed that the alveolar sacs gradually deflate until they are no longer providing adequate gas exchange. In order to reinflate the alveolar sacs, an individual must sigh, reinflating the alveolar sacs to their full size. Failure to periodically sigh can be fatal because normal breaths allow the alveolar sacs to slowly deflate.